Neurological Research (NEUROL RES )

Publisher: Maney Publishing

Description

Neurological Research is an international peer-reviewed journal publishing original and fundamental studies as well as clinical research in areas of neurology, neurosurgery and neurosciences, together with such subspecialty areas as: neuro-oncology, neuropsychiatry, neurotraumatology, neuroradiology, neuropathology and molecular biology. Each issue comprises articles of clinical significance and scientific excellence with original research, case reports, and broad-based review articles, with rapid publication turnaround.

  • Impact factor
    1.18
    Show impact factor history
     
    Impact factor
  • 5-year impact
    1.34
  • Cited half-life
    7.40
  • Immediacy index
    0.23
  • Eigenfactor
    0.01
  • Article influence
    0.36
  • Website
    Neurological Research website
  • Other titles
    Neurological research
  • ISSN
    0161-6412
  • OCLC
    3983345
  • Material type
    Periodical
  • Document type
    Journal / Magazine / Newspaper

Publisher details

Maney Publishing

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • On author's personal or institutional web site, or institutional repository
    • Must link to publisher version
    • Publisher copyright and source must be acknowledged
    • On a non-profit server
    • Pre-print must be replaced by post-print version upon publication
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Objective: Cerebral hyperperfusion syndrome (HPS) is a potential complication of extracranial-intracranial (EC-IC) bypass for moyamoya disease; however, the pathological threshold of the early cerebral blood flow (CBF) increases after EC-IC bypass has yet to be determined. The purpose of this study is to evaluate the predictive and diagnostic values of early quantitative CBF analysis for the detection of HPS after EC-IC bypass for moyamoya disease. Methods: We quantitatively evaluated regional CBF at the site of the anastomosis in 23 patients with moyamoya disease aged between 18 and 66 years (mean, 39·6) before and 1 day after superficial temporal artery-middle cerebral artery anastomosis by an auto-radiographic method using N-isopropyl-p-[(123)I]iodoamphetamine single-photon emission computed tomography. Results: Regional CBF 1 day after surgery was significantly higher in patients with HPS (n = 5; mean, 54·6 ml/100 g/minutes) than in patients without HPS (n = 18; mean, 40·5 ml/100 g/minutes) (P = 0·038). The postoperative/preoperative CBF ratio was significantly higher in patients with HPS (1·84) than in patients without HPS (1·34) (P = 0·044). Multivariate analyses showed that the regional CBF value 1 day after surgery (P = 0·036) and operating on the left hemisphere (P = 0·026) significantly correlated with HPS. All patients with HPS developed symptoms and/or intracerebral hemorrhage more than 2 days after EC-IC bypass. Receiver operating characteristic analysis indicated that the cutoff value of pathological postoperative CBF increase was 46·1 ml/100 g/minutes (sensitivity = 80%, specificity = 77·8%, AUC value = 0·81). Conclusion: Quantitative analysis of early postoperative CBF is useful for predicting and diagnosing HPS after revascularization surgery for moyamoya disease.
    Neurological Research 08/2014;
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    ABSTRACT: Although neurovascular confliction was believed to be the cause of hemifacial spasm (HFS), the mechanism of the disorder remains unclear to date. Current theories, merely focusing on the facial nerve, have failed to explain the clinical phenomenon of immediate relief following a successful microvascular decompression surgery (MVD). With the experience of thousands of microvascular decompression surgeries and preliminary investigations, we have learned that the offending artery may play a more important role than the effect of merely mechanical compression in the pathogenesis of the disease. We believe that the attrition of neurovascular interface is the essence of the etiology, and the substance of the disease is emersion of ectopic action potentials from the demyelinated facial nerve fibers, which were triggered by the sympathetic endings from the offending artery wall. In this paper, we put forward evidence to support this hypothesis, both logically and theoretically.
    Neurological Research 07/2014;
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    ABSTRACT: Background: Alzheimer's disease (AD) is one of the most common dementia, which is not effectively cured to date. Amyloid-beta (Abeta) deposition cascade and disintegrity of brain extracellular matrix (ECM) scaffold attribute to the progress of AD. Thus, it maybe an effective way to treat AD by altering the processing of amyloid precursor protein (APP) and regaining the integrity of ECM. The peptide amphiphile (PA) with a laminin epitope isoleucine-lysine-valine-alanine-valine (IKVAV) (IKVAV-PA) can be trigged into ECM in vivo. In addition, IKVAV-PA could significantly improve cognitive impairment with remarkable increase of endoneurogensis in the hippocampus, as well as reduction of burden of amyloid plaque in the brain. Methods: We used heterozygous AbetaPPswe/PS1dE9 double transgenic mice as the animal model of AD. After 1 week of initial stereotaxic administration into bilateral hippocampus, the mice were subjected to the Morris Water Maze (MWM) test. At the end of MWM test, immunohistochemical staining, Western blot and real-time polymerase chain reaction (PCR) were performed in mice. Results: Here we showed that IKVAV-PA significantly improved cognitive impairment accompanying with reducing the burden of Abeta plaques, as well as the levels of soluble Abeta1-40 and Abeta1-42 in the cortex and hippocampus after 2 weeks of initial administration into bilateral hippocampus. Further examination demonstrated that IKVAV-PA also altered the processing of APP via inhibiting the gene expression of beta-secretase (BACE1), as well as improving the gene expression of insulin-degrading enzyme (IDE) and neprilysin (NEP). Conclusion: Our data suggest that IKVAV-PA may serve as an alternative therapeutic intervention for treating the learning and memory losses in AD.
    Neurological Research 07/2014;
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    ABSTRACT: Aim: Parkinson's disease (PD) patients frequently present visual hallucinations (VHs) that have been associated with depression, old age, and cognitive impairment. Sleep abnormalities are also related to these factors. The aim of this study is to evaluate risk factors, particularly sleep alterations, associated with VHs in PD. Methods: This is a cross-sectional evaluation of consecutive patients from a Movement Disorder's clinics. Patients were clinically evaluated, and behavioral questionnaires were applied in a face-to-face interview. Results: Among 100 PD patients (67% male, mean age = 65·0 ± 10·4), VHs were present in 28% of cases; individuals with VHs had worse sleep quality (Pittsburgh Sleep Questionnaire Index) and more severe sleep disturbances [Parkinson's Disease Sleep Scale (PDSS)]. Logistic regression analysis showed that vivid dreams and Unified Parkinson's Disease Rating Scale (UPDRS) I scores (i.e., mentation, behavior, and mood symptoms) are independently associated with VHs. Our data show that the presence of vivid dreams is associated with VHs in PD and reaffirm that VHs are linked to cognitive impairment. Conclusions: Investigating vivid dreams may help the identification of VHs in PD. Identifying vivid dreams can be hard considering that patients may fail to report symptoms for the fear of the stigma associated with psychosis and dementia.
    Neurological Research 07/2014;
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    ABSTRACT: Objective: To determine if a computer-based simulation with haptic technology can help surgical trainees improve tactile discrimination using surgical instruments. Material and Methods: Twenty junior medical students participated in the study and were randomized into two groups. Subjects in Group A participated in virtual simulation training using the ImmersiveTouch simulator (ImmersiveTouch, Inc., Chicago, IL, USA) that required differentiating the firmness of virtual spheres using tactile and kinesthetic sensation via haptic technology. Subjects in Group B did not undergo any training. With their visuals fields obscured, subjects in both groups were then evaluated on their ability to use the suction and bipolar instruments to find six elastothane objects with areas ranging from 1·5 to 3·5 cm(2) embedded in a urethane foam brain cavity model while relying on tactile and kinesthetic sensation only. Results: A total of 73·3% of the subjects in Group A (simulation training) were able to find the brain cavity objects in comparison to 53·3% of the subjects in Group B (no training) (P = 0·0183). There was a statistically significant difference in the total number of Group A subjects able to find smaller brain cavity objects (size ≤ 2·5 cm(2)) compared to that in Group B (72·5 vs 40%, P = 0·0032). On the other hand, no significant difference in the number of subjects able to detect larger objects (size ≧ 3 cm(2)) was found between Groups A and B (75 vs 80%, P = 0·7747). Conclusion: Virtual computer-based simulators with integrated haptic technology may improve tactile discrimination required for microsurgical technique.
    Neurological Research 07/2014;
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    ABSTRACT: Objectives: Postconditioning with sevoflurane has been shown to protect against focal cerebral ischemia and reperfusion injury. However, the mechanism remains elusive. In this study, we tested the hypothesis that mitochondrial ATP-sensitive potassium (mitoKATP) and mitochondrial permeability transition pore (mPTP) play roles in the neuroprotection of postconditioning with sevoflurane. Methods: Adult male Sprague-Dawley rats were subjected to MCAO for 90 minutes and then treated with sevoflurane at the beginning of reperfusion. The infarct volume, neurological deficit score, and brain edema were evaluated at 24 hours. Apoptosis were studied by TUNEL. The neuroprotective effect with or without 5-hydroxydecanoate (5-HD), a selective mitoKATP channel blocker or atractyloside (ATR), and an mPTP opener were analyzed. Results: Postconditioning with sevoflurane significantly decreased neurological deficit scores, infarct volume, and brain edema and also reduced apoptotic cells. 5-HD and ATR abolished the neuroprotective effect, respectively. 5-HD or ATR alone had no effect on ischemia and reperfusion injury. Discussion: Our data suggest that mitoKATP and mPTP play crucial roles in the neuroprotection of postconditioning with sevoflurane.
    Neurological Research 06/2014;
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    ABSTRACT: Objectives: Restenosis or neointimal hyperplasia remains an important complication after carotid artery stenting (CAS) for carotid artery stenosis. The purpose of this study was to examine if an anti-hypertensive drug, angiotensin receptor blocker (ARB), prevents post-CAS neointimal hyperplasia during the first 1-year period after CAS, and to clarify the possible mechanisms. Methods: Hypertension had been treated with a calcium channel blocker (CCB) and/or an ARB, valsartan, by the preference of the neurosurgeon in charge in our department. At admission to perform CAS, patients were assigned to normotensive, valsartan (hypertensive patients treated with valsartan with/without any kind of CCBs), and non-valsartan (hypertensive patients treated with any kind of CCBs without ARBs) groups. Post-CAS neointimal hyperplasia was evaluated by carotid duplex ultrasound imaging in terms of intima-media thickening (IMT), which was performed at pre-CAS and at 90, 180, 270, and 360 days post-CAS. Biomarkers of oxidative stress (8-hydroxy-2'-deoxyguanosine), inflammation (C-reactive protein, tenascin-C) and endothelial cell injury (von Willebrand factor [vWF] antigen) were measured at pre-CAS and at 1, 7, and 180 days post-CAS. Results: The non-valsartan group (n = 8) had a higher incidence of maximum in-stent IMT ≧ 1·1 mm compared with the normotensive group (n = 6). Valsartan (n = 9) significantly suppressed plasma vWF levels at 7 days post-CAS and decreased the incidence of maximum in-stent IMT ≧ 1·1 mm compared with the non-valsartan group, although clinical parameters were similar between the two groups. Other biomarkers were not significantly different among the three groups. Conclusions: These findings suggest that valsartan may prevent post-CAS neointimal hyperplasia possibly by suppressing endothelial cell injury.
    Neurological Research 06/2014;
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    ABSTRACT: Objective: Brain-derived neurotrophic factor (BDNF) binds to its high-affinity binding receptor, tropomyosin-related kinase (Trk) B, and can induce neuronal differentiation and survival. BDNF also accelerates neuronal cell death in a glutamate-induced model; however, it has been unknown whether the mechanism involves TrkB. In the current study, to determine the role of TrkB in neuronal cell death, we investigated TrkB involvement in BDNF acceleration of glutamate-induced neuronal death. Methods: A TrkB-stable transformant of rat neuroblastoma B35 (B35(TrkB)) cells was utilized to investigate whether TrkB is involved in BDNF acceleration of neuronal death. The cell viability of the B35(TrkB) cells was compared to that of mock vector-transgened B35 (B35(mock)) cells after treatment with/without BDNF and glutamate. Results: In both B35(TrkB) and B35(mock) cells, glutamate treatment decreased the cell viability. BDNF treatment further accelerated the decrease in the viability of B35(TrkB) cells, but not that in the viability of B35(mock) cells. At glutamate concentrations that did not significantly decrease cell viability, BDNF increased the cell viability of B35(TrkB), but not that of B35(mock). A mitogen-activated protein kinase (MAPK) inhibitor, U0126, suppressed BDNF's accelerating effect on cell death. Although B35 parental cells endogenously express other neurotrophin receptors such as TrkA, nerve growth factor β (a ligand of TrkA and p75(NTR)) could not influence the viability of B35(TrkB) or B35(mock) cells. Conclusion: These results indicate that TrkB is an intermediator for the trophic and toxicity-exacerbating effects of BDNF against cell viabilities at non-cytotoxic and cytotoxic glutamate concentrations, respectively.
    Neurological Research 06/2014;
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    ABSTRACT: Background and Purpose: Painful vertebral compression fractures in cancer patients reduce quality of life and may limit survival. We assessed pain relief, vertebral height restoration, and kyphosis correction following vertebral augmentation using a novel expandable titanium stent implant in cancer patients with painful vertebral compression fractures. Materials and Methods: Patients >18 years of age with metastatic disease who presented symptomatic compression fractures of vertebral bodies T5-L5, with or without a history of osteoporosis, were included in the study. Back pain at presentation, immediately after vertebral stenting, and at 1-, 3-, 6-, and 12-month follow-up was estimated using the visual analog scale (VAS). Vertebral height and local kyphotic angle (alpha angle) were measured on lateral standing X-ray before and 1-3 months after stenting. Results: Forty-one cancer patients with painful vertebral compression fractures underwent vertebral stenting procedures at 55 levels. There was no perioperative mortality and no significant complication. Median preoperative VAS was 8·0 (range 8-10), falling to 2·0 immediately postop (range 1-6, P = 0·000) and 0 at all subsequent follow-up (P ≤ 0·012). Mean preoperative vertical height loss was 25·8% (range 0-84·0%) versus a postoperative mean of 18·0% (range 0-66·0%, P = 0·000). Median pre- and postoperative kyphotic angle improved from 8·3° (range 0·2°-54·0°) to 7·1° (range 0·2°-25·0°, P = 0·000). Wilcoxon signed rank test or student's t-test was used for comparisons. Conclusions: Vertebral augmentation using a novel vertebral stenting system provided immediate and enduring pain relief and improved vertebral height loss and kyphotic angle.
    Neurological Research 06/2014;
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    ABSTRACT: Objectives: The partial pressure of oxygen (pO2) in brain tumors ranges from 5 to 15%. Nevertheless, the majority of in vitro experiments with glioblastoma multiforme (GBM) cell lines are carried out under an atmospheric pO2 of 19 to 21%. Recently, 5-aminolevulinic acid (5-ALA), a precursor of protoporphyrin IX (PpIX), has been introduced to neurosurgery to allow for photodynamic diagnosis and photodynamic therapy (PDT) in high-grade gliomas. Here, we investigate whether low pO2 affects GBM cell physiology, PpIX accumulation, or PDT efficacy. Methods: GBM cell lines (U-87 MG and U-251 MG) were cultured under atmospheric (pO2 = 19%) and physiological (pO2 = 9%) oxygen concentrations. PpIX accumulation and localization were investigated, and cell survival and cell death were observed following in vitro PDT. Results: A physiological pO2 of 9% stimulated GBM cell migration, increased hypoxia-inducible factor (HIF)-1 alpha levels, and elevated resistance to camptothecin in U-87 MG cells compared to cultivation at a pO2 of 19%. This oxygen reduction did not alter 5-ALA-induced intracellular PpIX accumulation. However, physiological pO2 changed the responsiveness of U-87 MG but not of U-251 MG cells to in vitro PDT. Around 20% more irradiation light was required to kill U-87 MG cells at physiological pO2, resulting in reduced lactate dehydrogenase (LDH) release (one- to two-fold) and inhibition of caspase 3 activation. Discussion: Reduction of oxygen concentration from atmospheric to a more physiological level can influence the malignant behavior and survival of GBM cell lines after in vitro PDT. Therefore, precise oxygen concentration control should be considered when designing and performing experiments with GBM cells.
    Neurological Research 06/2014;
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    ABSTRACT: Transplanted human umbilical cord mesenchymal stem cells (hUC-MSCs) have exhibited considerable therapeutic potential for traumatic brain injury (TBI). However, how hUC-MSCs migrating to the injury region and the mechanism of hUC-MSCs promoting functional recovery after TBI are still unclear. In this study, we investigated whether stromal cell-derived factor-1 (SDF-1) was involved in the hUC-MSCs migration and the possible mechanisms that might be involved in the beneficial effect on functional recovery. In vitro experiments demonstrated that SDF-1 induces a concentration-dependent migration of hUC-MSCs. Furthermore, pre-treatment with the CXCR4-specific antagonist AMD3100 significantly prevented the migration of hUC-MSCs in vitro. We found that the expression of SDF-1 increased significantly around the damaged area. Transplanted hUC-MSCs were localized to regions where SDF-1 was highly expressed. Additionally, our results showed that hUC-MSCs-treated animals showed significantly improved functional recovery compared with controls. In hUC-MSCs-transplanted group, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL)-positive cells were decreased and BrdU-positive cells were significantly increased compared with control group, more of BrdU-positive cells co-localized with GFAP. These suggest that SDF-1 plays an important role in the migration of hUC-MSCs to the damaged area and hUC-MSCs are beneficial for functional recovery after TBI.
    Neurological Research 06/2014;
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    ABSTRACT: Deficiency of vitamin B12 produces protean effects on the nervous system, most commonly neuropathy, myelopathy, cognitive and behavioural symptoms, and optic atrophy. Involuntary movements comprise a relatively rare manifestation of this readily treatable disorder. Both adults and infants deficient in vitamin B12 may present with chorea, tremor, myoclonus, Parkinsonism, dystonia, or a combination of these, which may precede diagnosis or become apparent only a few days after parenteral replacement therapy has begun. The pathogenesis of these movement disorders shows interesting parallels to certain neurodegenerative conditions. The clinical syndrome responds well to vitamin B12 supplementation in most cases, and an early diagnosis is essential to reverse the haematological and neurological dysfunction characteristic of this disorder. In this article, we elucidate the association of vitamin B12 deficiency with movement disorders in adults and in infants, discuss the pathogenesis of this association, review previously reported cases, and present a young adult male with severe generalized chorea that showed a salutary response to vitamin B12 supplementation.
    Neurological Research 05/2014;
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    ABSTRACT: Objective: We investigated whether a correlation exists between insulin resistance and the severity of cerebral white matter lesions among non-diabetic patients with ischemic stroke.Methods: The subjects were 105 consecutive patients without diabetes who were hospitalized due to non-cardioembolic stroke. The insulin resistance was evaluated by a homeostasis model assessment of insulin resistance (HOMA-IR). The degrees of periventricular hyperintensity (PVH) and deep and subcortical white matter hyperintensity (DSWMH) were evaluated by the brain MRI. The HOMA-IR values ?2?5 were indicative of the insulin resistance.Results: The presence of PVH and DSWMH were 86?7 and 83?8%, respectively. The ratio of insulin resistance increased with higher grades of PVH and DSWMH. The HOMA-IR level in grade 3 PVH was significantly higher than those in grades 0 and 1. The HOMA-IR level in grade 3 DSWMH was significantly higher than those in grades 0?2. Multiple linear regression analysis showed that HOMA-IR was significantly associated with PVH or DSWMH.Conclusion: It was found that insulin resistance correlated with white matter lesions among non-diabetic patients with non-cardiogenic ischemic stroke.Objective: We investigated whether a correlation exists between insulin resistance and the severity of cerebral white matter lesions among non-diabetic patients with ischemic stroke.Methods: The subjects were 105 consecutive patients without diabetes who were hospitalized due to non-cardioembolic stroke. The insulin resistance was evaluated by a homeostasis model assessment of insulin resistance (HOMA-IR). The degrees of periventricular hyperintensity (PVH) and deep and subcortical white matter hyperintensity (DSWMH) were evaluated by the brain MRI. The HOMA-IR values ?2?5 were indicative of the insulin resistance.Results: The presence of PVH and DSWMH were 86?7 and 83?8%, respectively. The ratio of insulin resistance increased with higher grades of PVH and DSWMH. The HOMA-IR level in grade 3 PVH was significantly higher than those in grades 0 and 1. The HOMA-IR level in grade 3 DSWMH was significantly higher than those in grades 0?2. Multiple linear regression analysis showed that HOMA-IR was significantly associated with PVH or DSWMH.Conclusion: It was found that insulin resistance correlated with white matter lesions among non-diabetic patients with non-cardiogenic ischemic stroke.
    Neurological Research 08/2010; 32(7):743-747.
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    ABSTRACT: Objective: The objective of this work was to understand how the baseball bat is a silent weapon. The baseball bat has been utilized illegally in different areas of the world. In the past, several case reports are known for their lethal effect. In this paper, we analyse the outcome of the utilization of baseball bat for illegal purposes as well as review the principal injury and the utilization of baseball bat as explained by an engineer.Material and Method: The medical and radiographic records of patients admitted to Sinai-Grace and Detroit Receiving Hospitals in Detroit, MI, USA, from June 1997 to June 2000, were reviewed. Ninety patients presented with documented baseball bat injury by history. Clinical data were obtained from the patients charts. Detailed descriptions of those body parts affected by baseball bat injury were registered and classified by anatomical regions.Results: A total of 39 cranial fractures were observed, mainly on the skull base and orbital wall.Discussion: Baseball bat-related injury is an endemic problem in Detroit. This urban use of the baseball bat as a weapon is getting severe. A team approach to this type of injury is recommended.
    Neurological Research 11/2009; 31(10):1005-1011.
  • Neurological Research 11/2009; 31(8):773-4.
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    ABSTRACT: To determine whether fasting would affect the frequency of cerebral venous and sinus thrombosis compared to other months. All patients (n=162) with cerebral venous and sinus thrombosis admitted to three neurological centers from 2001 to 2006 in the Isfahan City were included in this study. Patients were divided into two groups according to the month of onset of cerebral venous and sinus thrombosis. The first group included patients with cerebral venous sinus thrombosis that occurred while fasting (n=33) and the second group was composed of patients with onset in other months, while not fasting (n=129). We evaluated the number of cases per month and compared ages, gender and the distribution of new cases during fasting versus non-fasting months. From 2001 to 2006, the mean number of patients' diagnosis during fasting month was 5.5 versus mean number of patients during all other non-fasting months that was 1.95. The analysis showed a significantly increased frequency of cerebral venous sinus thrombosis events in Ramadan compared to other months (p=0.000). Our findings indicate that fasting increases frequency of cerebral venous and sinus thrombosis. These findings are inconsistent with other reported studies on arterial stroke and need to be confirmed by other studies. It seems that healthy people have no problem with regard to cerebral venous and sinus thrombosis while fasting, but susceptible persons, such as those with hypercoagulable states and women who take oral contraceptive pills, may be at increased risk.
    Neurological Research 11/2009; 31(8):794-8.
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    ABSTRACT: The objective of this study is to review the role of cell-derived microparticles in ischemic cerebrovascular diseases. An extensive PubMed search of literature pertaining to this study was performed in April 2009 using specific keyword search terms related to cell-derived microparticles and ischemic stroke. Some references are not cited here as it is not possible to be all inclusive or due to space limitation. Cell-derived microparticles are small membranous vesicles released from the plasma membranes of platelets, leukocytes, red cells and endothelial cells in response to diverse biochemical agents or mechanical stresses. They are the main carriers of circulating tissue factor, the principal initiator of intravascular thrombosis, and are implicated in a variety of thrombotic and inflammatory disorders. This review outlines evidence suggesting that cell-derived microparticles are involved predominantly with microvascular, as opposed to macrovascular, thrombosis. More specifically, cell-derived microparticles may substantially contribute to ischemic brain disease in several settings, as well as to neuroinflammatory conditions. If further work confirms this hypothesis, novel therapeutic strategies for minimizing cell-derived microparticles-mediated ischemia are available or can be developed, as discussed.
    Neurological Research 11/2009; 31(8):799-806.
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    ABSTRACT: The current review covers causes and risk factors of vascular dementia, including single infarct, multi-infarct and cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy. Comparisons and distinctions are made between vascular dementia and Alzheimer's dementia, including shared vascular features and risk factors, differential diagnosis based on presenting history, neuropsychological testing results and neuroimaging findings. Neuropsychological findings associated with vascular dementia are discussed, and efforts towards stroke prevention and limiting the recurrence of stroke, as well as emerging treatment possibilities for cognitive decline associated with vascular dementia, are presented. A PubMed-based literature review was performed to acquire recent peer-reviewed publications on vascular dementia. Stroke is one of the leading causes of disability, dementia and death. Within the USA, roughly 660,000 persons will experience a stroke each year. Although many individuals go on to demonstrate substantial improvement and recovery following stroke, a substantial percentage show residual effects including dementia. Vascular dementia has variable causes and manifestations, and research is revealing increasingly more common ground between vascular dementia and Alzheimer's dementia. However, vascular dementia often remains clinically distinct from Alzheimer's dementia, and profiles of neuropsychological impairment can be used to differentiate vascular dementia from the more common Alzheimer's dementia with some success. Vascular dementia causes dependence and disability. Most stroke survivors show improvement, but many develop dementia. Understanding for vascular dementia has recently improved, leading to improved treatment planning. Further research, especially on treatment for vascular dementia, is greatly needed.
    Neurological Research 11/2009; 31(8):824-31.

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